Th17 Cells and Autoimmune Encephalomyelitis (EAE/MS)

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  • Aranami Toshimasa
    Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry
  • Yamamura Takashi
    Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry

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Multiple sclerosis (MS) is a CD4+ T cell-mediated autoimmune disease affecting the central nervous system. It was largely accepted that Th1 cells driven by IL-12 were pathogenic T cells in human MS and experimental autoimmune encephalomyelitis, an animal model of MS. Recent data have established that IL-17-producing CD4+ T cells, driven by IL-23 and referred to as Th17 cells, play a pivotal role in the pathogenesis of EAE. A combination of TGF-β and IL-6 induce Th17 cell lineage commitment via expression of transcription factor RORγt. Th17 cells and induced Foxp3+ T regulatory cells are in reciprocal position in the T cell lineage commitment governed by TGF-β and IL-6. The vitamin A metabolite retinoic acid is involved in this process via TGF-β dependent induction of Foxp3. We have demonstrated that human Th17 cells could be identified as CCR2+ CCR5- memory CD4+ T cells. It is becoming clear that IL-23/Th17 axis also plays an important role in the pathogenesis of various human autoimmune diseases including MS. Additionally, accumulating evidences raise a possibility that CCR2 on Th17 cells may be a therapeutic target in MS.<br>

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